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ANEMONES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Anemones are found in the phylum Coelenterata, class Anthozoa. They are very abundant, with over 1000 species which may live in tropical to arctic waters in depths ranging from the tidal zone to over 5000 feet deep (Halstead, 1978).
    B) Size: Can range from 0.5 meter to only a few millimeters, and generally, nonmotile organs that attach to some other object. They have stalked, finger-like projections that have "flower-like tentacles" covered (capsules) with nematocysts used for stinging and paralyzing fish (McGoldrick & Marx, 1992; Fisher, 1999).
    C) Some anemones are venomous coelenterates which can sting humans, by using the nematocysts on the tentacles. Nematocysts are sensitive to both chemical and mechanical stimulation (Pantin, 1942). Venom is transferred from the nematocyst capsule through a tube, and into the victim (Halstead, 1978) Fisher, 1999).
    D) Some anemones are poisonous when ingested, but it is unknown if this is a nematocyst induced reaction, or due to some other toxin (Tu, 1988).

Specific Substances

    A) Actinia equina
    1) Sea Anemone
    Actinodendron plumosum
    1) Actinarian
    2) Actinodendron alcyonoideum
    3) Actinodendron arboreum
    4) Hell's fire sea anemone
    5) Stinging anemone
    Anemonia sulcata
    1) Actinia sulcata
    Adamsia palliata
    1) Anthea cerus
    Physobrachia douglasi
    1) Gyrostoma kraemeri
    2) Junior homonym
    Rhodactis howesii
    1) Malu-Malu
    Sagartia elegans
    1) Rosy anemone
    2) Sagartia rosea
    STICHACTIS HELIANTHUS
    1) Stichodactyla helianthus
    Turtle grass anemone
    1) Viatrix globulifera

Available Forms Sources

    A) SOURCES
    1) ILLNESS - Maladie des plongeurs (sponge fisherman's disease) is caused by anemones. As the workers gather the sponges, they brush off stones and other debris and hang the sponges on their necks. In the process they may be stung by anemones clinging to the sponges (Zervos, 1934; (Phisalix, 1922; Evans, 1943; Southcott, 1952).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Anemones are sessile marine creatures that have nematocysts on their fronds and sting on contact. They are found throughout the world in temperate and tropical waters.
    B) TOXICOLOGY: The venoms are complex mixtures of enzymes and proteins. Pain is likely caused by fractions that induce histamine release, and dermal injury by fractions that contain cytolysins.
    C) EPIDEMIOLOGY: Anemones are quite beautiful and are widely photographed. Divers and snorkelers are at particular risk from touching or brushing against fronds, or coming into contact with extruded nematocysts. The majority of exposures only cause pain and localized dermal reactions.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE: Contact with nematocysts generally produces an intense stinging and burning sensation. Small papules with surrounding erythema are common. More severe dermal reactions can include larger vesicles, bullae, local discoloration and scarring. Some patients may develop systemic effects such as vomiting, abdominal pain, malaise, dizziness, headache, chills and fever.
    2) SEVERE: Acute renal failure and hepatic failure are very rare, but have been reported.
    3) INGESTION: If the brown or green anemone Rhodactis howesii has been ingested, the patient may first become agitated or confused, then delirious and finally comatose. Hypotension, fever, respiratory failure, and seizures may also develop.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) No specific laboratory evaluation is needed for the majority of patients.
    B) For patients with severe persistent symptoms monitor renal function, liver enzymes, coagulation studies and CBC.
    C) Monitor the area of the sting for evidence of secondary infection.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) SUMMARY
    1) If raw or poorly cooked Rhodactis howesii has been ingested, gastric decontamination should be considered. There have been few cases of seizures after ingestion.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) WOUND TREATMENT
    a) Wash the affected area with sea water and remove any fronds with a stick, knife, or forceps (avoid fresh water until nematocysts are removed as it may trigger firing).
    b) Remove remaining nematocysts manually. One recommended method is to apply shaving cream, or a paste of baking soda or flour, to the area and scrape off remaining nematocysts with the edge of a sharp knife (caregivers should wear gloves and avoid direct contact with nematocysts.
    c) Immersion of the affected area in hot water (113 F or 45 C) for up to 20 minutes has been shown to decrease pain and prevent recurrence of pain with some jellyfish stings, it is not known if this is effective for anemone stings. Immersion is preferred over a hot water shower as it provides a more consistent temperature and contact with the skin.
    d) Apply a corticosteroid, antihistamine, or local anesthetic cream such as Itch Balm Plus(R) for several days.
    2) ANTIHISTAMINES: Oral and topical antihistamines have been used as treatment for the rash and pruritus.
    3) CORTICOSTEROIDS: Dermatitis may be treated with topical corticosteroids.
    4) Patients with more severe reactions may require oral NSAIDs or narcotic analgesics and oral corticosteroids.
    5) PATIENT DISPOSITION
    a) HOME CRITERIA: Patients with mild to moderate pain can be managed at home with dermal decontamination.
    b) OBSERVATION CRITERIA: Patients with severe pain should be referred to a healthcare facility for evaluation.
    c) ADMISSION CRITERIA: Rarely, patients with systemic complications or intractable pain will require admission.
    d) CONSULT CRITERIA: Consult a toxinologist, medical toxicologist or poison center for patients with severe stings or in whom the diagnosis is unclear.
    6) PITFALLS
    a) Can be difficult to distinguish from other marine envenomations.
    7) TOXICOKINETICS
    a) Onset of pain is generally quite rapid, within 15 minutes. Skin lesions commonly resolve over several days.
    8) DIFFERENTIAL DIAGNOSIS
    a) Sting from a jellyfish, coral or fish, contact or irritant dermatitis, zoster.

Range Of Toxicity

    A) TOXICITY: The sting of a single anemone may produce significant symptoms that generally resolve within a few days. Fatalities are extremely rare, but a death from hepatic and renal failure after anemone sting has been reported. Death has been reported after ingestion of raw Rhodactis howesii.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Anemones are sessile marine creatures that have nematocysts on their fronds and sting on contact. They are found throughout the world in temperate and tropical waters.
    B) TOXICOLOGY: The venoms are complex mixtures of enzymes and proteins. Pain is likely caused by fractions that induce histamine release, and dermal injury by fractions that contain cytolysins.
    C) EPIDEMIOLOGY: Anemones are quite beautiful and are widely photographed. Divers and snorkelers are at particular risk from touching or brushing against fronds, or coming into contact with extruded nematocysts. The majority of exposures only cause pain and localized dermal reactions.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE: Contact with nematocysts generally produces an intense stinging and burning sensation. Small papules with surrounding erythema are common. More severe dermal reactions can include larger vesicles, bullae, local discoloration and scarring. Some patients may develop systemic effects such as vomiting, abdominal pain, malaise, dizziness, headache, chills and fever.
    2) SEVERE: Acute renal failure and hepatic failure are very rare, but have been reported.
    3) INGESTION: If the brown or green anemone Rhodactis howesii has been ingested, the patient may first become agitated or confused, then delirious and finally comatose. Hypotension, fever, respiratory failure, and seizures may also develop.

Vital Signs

    3.3.3) TEMPERATURE
    A) Both fever and chills have been reported after anemone stings (Halstead, 1978).
    B) FEVER has been reported after ingestion of Rhodactis howesii (Tu, 1988).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been reported after ingestion of Rhodactis howesii (Tu, 1988).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSRHYTHMIA
    a) Experiments in animals using the purified protein venom from Anemonia sulcata produced dysrhythmias and decreased arterial blood pressure (Novak et al, 1973).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) Respiratory failure has been reported after ingestion of Rhodactis howesii (Tu, 1988).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) MICE: Injection of Anemonia sulcata venom into mice caused respiratory and cardiac arrest (Alsen et al, 1978).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) MALAISE
    1) WITH POISONING/EXPOSURE
    a) Malaise is sometimes reported after sea anemone stings (Halstead, 1978).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may develop after stings by anemones (Halstead, 1978).
    C) COMA
    1) WITH POISONING/EXPOSURE
    a) ANEMONE INGESTION POISONING: If the brown or green anemone Rhodactis howesii has been ingested, the patient first becomes agitated or confused, then delirious and finally comatose (Tu, 1988). Seizures may also occur (Tu, 1988).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and abdominal pain may occur after the sting of anemones (Maretic & Russell, 1983; Halstead, 1978).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain has been reported after ingestion of Rhodactis howesii (Tu, 1988).
    C) THIRST FINDING
    1) WITH POISONING/EXPOSURE
    a) Extreme thirst may accompany an anemone sting (Halstead, 1978).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) HEPATIC FAILURE
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: There is limited evidence that hepatic failure may develop following sea anemone stings.
    b) CASE REPORT: Hepatic failure developed in an adult male 3 days after envenomation by a sea anemone. Liver enzyme levels were elevated 24 hrs following the sting, and remained elevated by day 5 after the sting. The patient did not survive a liver and kidney transplant. Massive hepatic necrosis, with diffuse peripheral lobular regeneration were identified in the explanted liver (Garcia et al, 1994).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: There is limited evidence that renal failure may result from sea anemone stings.
    b) CASE REPORT: Oliguric renal failure and acute hepatic failure developed in an adult who was stung by a sea anemone. Mild tubular necrosis was identified by postmortem renal biopsy (Garcia et al, 1994).
    c) CASE REPORT: A 27-year-old man developed severe swelling and pain in his arm after touching an anemone. He presented to a hospital 2 days later with a creatinine of 4.6 mg/dL and a BUN of 54 mg/dL. His CK was 648 Units/L, serum myoglobin 57.5 ng/mL (peaked at 94.6 ng/mL 4 days after the sting) and urinalysis showed 30 mg/dL protein and glucose, trace blood and normal sediment. He was not oliguric, renal biopsy was consistent with acute tubular necrosis, and renal function returned to normal by the 4th day of hospitalization (Mizuno et al, 2000).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) The venom of the sea anemone Aiptasia pallida has been shown to exhibit phospholipase A activity on red cell membrane phospholipids (Halstead, 1978; pp 379-383). Hemolysis has not been reported in humans after a sting.
    B) BLOOD COAGULATION PATHWAY FINDING
    1) WITH POISONING/EXPOSURE
    a) Delays in prothrombin time and partial thromboplastin time were associated with a sea anemone sting in a human (Garcia et al, 1994).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Bundosoma caissarum venom has been shown to have hemolytic activity in the fish, toad, snake, mouse, and rat. Sphingomyelin is the possible hemolysin acceptor (Freitas & Malpezzi, 1991).
    b) Various Heteractis, Stoichactis, and Gyrostoma species have been shown to hemolyze human erythrocytes (Claus I, Schroter A & Mebs D et al, 1991).
    c) Equinatoxin II is a hemolytic, cytotoxic protein from Actinia equina (Komatsu et al, 1992).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) PAIN
    1) WITH POISONING/EXPOSURE
    a) Contact with anemone nematocysts causes almost immediate pain that is described as stinging or burning, and may be quite intense (Sanchez-Rodriguez et al, 2001; Nicholls, 1992; Maretic & Russell, 1983).
    b) Skin pain after ingestion of Rhodactis howesii has been reported. Touching the skin, or especially the mucous membranes, may be very painful (Tu, 1988).
    B) VESICULAR REACTION
    1) WITH POISONING/EXPOSURE
    a) The initial dermal reaction usually consists of blanched papules with surrounding erythema that develops within a few minutes of the sting. In minor cases this persists for several days and resolves spontaneously (Sanchez-Rodriguez et al, 2001; Maretic & Russell, 1983).
    b) With more severe stings, the lesions may become purplish over the subsequent few hours, bullae may develop and edema may become more generalized. The bullae or vesicles eventually rupture, to be replaced by an eschar. These wound heal more slowly and occasionally become secondarily infected. Permanent sequelae can include hyper or hypopigmentation and keloid formation (Maretic & Russell, 1983).
    C) SKIN NECROSIS
    1) WITH POISONING/EXPOSURE
    a) Symptoms after stings by sea anemones are usually limited to the site of sting with itching and burning. Symptoms can progress from redness and swelling to ulceration or local necrosis (Halstead, 1978).
    D) ABSCESS
    1) WITH POISONING/EXPOSURE
    a) Severe sloughing of affected tissues may occur, accompanied by a prolonged period of purulent discharge. Multiple abscesses have been observed (Halstead, 1978).
    1) The resulting ulcers are difficult to treat and take a long time to heal (Halstead, 1978).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Diffuse pain and myalgias have been reported after anemone stings, particularly in children (Maretic & Russell, 1983).
    b) Myalgias may develop after ingestion of Rhodactis howesii (Tu, 1988).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory evaluation is needed for the majority of patients.
    B) For patients with severe persistent symptoms monitor renal function, liver enzymes, coagulation studies and CBC.
    C) Monitor the area of the sting for evidence of secondary infection.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) No specific measures are indicated.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.5) DISPOSITION/DERMAL EXPOSURE
    6.3.5.1) ADMISSION CRITERIA/DERMAL
    A) Rarely, patients with systemic complications or intractable pain will require admission.
    6.3.5.2) HOME CRITERIA/DERMAL
    A) Patients with mild to moderate pain can be managed at home with dermal decontamination.
    6.3.5.3) CONSULT CRITERIA/DERMAL
    A) Consult a toxinologist, medical toxicologist or poison center for patients with severe stings or in whom the diagnosis is unclear.
    6.3.5.5) OBSERVATION CRITERIA/DERMAL
    A) Patients with severe pain should be referred to a healthcare facility for evaluation.

Monitoring

    A) No specific laboratory evaluation is needed for the majority of patients.
    B) For patients with severe persistent symptoms monitor renal function, liver enzymes, coagulation studies and CBC.
    C) Monitor the area of the sting for evidence of secondary infection.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) If raw or poorly cooked Rhodactis howesii has been ingested, gastric decontamination should be considered. There have been few cases of seizures after ingestion, so the risk of aspiration should be taken into consideration.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) EXPERIMENTAL THERAPY
    1) EXPERIMENTAL ANIMALS: Experiments with guinea pig hearts found that verapamil and nitroglycerin abolished the negative inotropic effects of equitoxin II and abolished the reduction of coronary flow. Verapamil prevented cardiac arrhythmias more effectively than did nitroglycerin (Budihna et al, 1991). This has not been tried in humans.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Wash the affected area with sea water and remove any fronds with a stick, knife, or forceps (avoid fresh water until nematocysts are removed as it may trigger firing).
    2) Remove remaining nematocysts manually. One recommended method is to apply shaving cream, or a paste of baking soda or flour, to the area and scrape off remaining nematocysts with the edge of a sharp knife (caregivers should wear gloves and avoid direct contact with nematocysts(Martin & Audley, 1990).
    3) VINEGAR: Some authors recommend exposures be irrigated with sea water (not fresh water) and then topical 5% acetic acid (vinegar) (McGoldrick & Marx, 1992).
    a) MEAT TENDERIZER (Proteolytic Enzymes): Application can help to neutralize toxins on the skin surface (Schwartz & Meinking, 1997).
    b) AVOID rinsing or showering in fresh water as this may result massive triggering of nematocysts and worsen envenomation (Schwartz & Meinking, 1997).
    6.9.2) TREATMENT
    A) SUPPORT
    1) Immersion of the affected area in hot water (113 F or 45 C) for up to 20 minutes has been shown to decrease pain and prevent recurrence of pain with some jellyfish stings, it is not known if this is effective for anemone stings. Immersion is preferred over a hot water shower as it provides a more consistent temperature and contact with the skin (Loten et al, 2006; Taylor, 2007).
    2) Apply a corticosteroid, antihistamine, or local anesthetic cream such as Itch Balm Plus(R) for several days.
    3) ANTIHISTAMINES: Oral and topical antihistamines have been used as treatment for the rash and pruritus (Halstead, 1980).
    B) CORTICOSTEROID
    1) Dermatitis may be treated with topical corticosteroids (McGoldrick & Marx, 1992), and persistent symptoms may require oral steroids given as a tapering dose (Schwartz & Meinking, 1997).
    C) TETANUS TOXOID
    1) A tetanus booster is recommended after envenomation (Schwartz & Meinking, 1997).
    D) PAIN
    1) Pain management may require NSAIDs or narcotic analgesics (Schwartz & Meinking, 1997).
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ADULT
    1) A 28-year-old man was stung on the back by an anemone while diving. He developed immediate pain and a vesicular reaction, and was admitted to a local hospital and treated with IV fluids and meperidine for 24 hours. After discharge he became more lethargic and weak, and was readmitted 24 hours later with jaundice and elevated liver enzymes. His neurologic status deteriorated and 5 days after the sting he was intubated and transferred to an intensive care setting. On arrival he was in fulminant hepatic failure (total bilirubin 6.7 mg/dL (115 micromol/L), AST 8692 units/L (145 microkat/L), ALT 9313 units/L (155 microkat/L), PT 75.2 seconds), and renal failure (BUN 42 mg/dL (15 mmol/L), creatinine 2.1 mg/dL (185 /micromol/L)). Evaluation for viral hepatitis and HIV were negative, and there was no history of exposure to other hepatotoxins. Over the next 3 days he became unresponsive, and he developed cerebral edema and oliguric renal failure. He died after receiving a liver and kidney transplant 4 days after being transferred. Serum obtained 8 days following the sting was positive (ELISA assay) for IgG specific to Condylactis sp. antigen. Biopsies of the explanted liver and kidneys revealed massive hepatic necrosis and mild renal tubular necrosis (Garcia et al, 1994).

Range Of Toxicity

Summary

    A) TOXICITY: The sting of a single anemone may produce significant symptoms that generally resolve within a few days. Fatalities are extremely rare, but a death from hepatic and renal failure after anemone sting has been reported. Death has been reported after ingestion of raw Rhodactis howesii.

Minimum Lethal Exposure

    A) STING
    1) CASE REPORT: A 28-year-old man was stung on the back by an anemone while diving. He developed immediate pain and a vesicular reaction, and was admitted to a local hospital and treated with IV fluids and meperidine for 24 hours. After discharge he became more lethargic and weak, and was readmitted 24 hours later with jaundice and elevated liver enzymes. His neurologic status deteriorated and 5 days after the sting he was intubated and transferred to an intensive care setting. On arrival he was in fulminant hepatic failure (total bilirubin 6.7 mg/dL (115 micromol/L), AST 8692 units/L (145 microkat/L), ALT 9313 units/L (155 microkat/L), PT 75.2 seconds), and renal failure (BUN 42 mg/dL (15 mmol/L), creatinine 2.1 mg/dL (185 /micromol/L)). Evaluation for viral hepatitis and HIV were negative, and there was no history of exposure to other hepatotoxins. Over the next 3 days he became unresponsive, and he developed cerebral edema and oliguric renal failure. He died after receiving a liver and kidney transplant 4 days after being transferred. Serum obtained 8 days following the sting was positive (ELISA assay) for IgG specific to Condylactis sp. antigen. (Garcia et al, 1994).
    B) INGESTION
    1) Deaths have been reported, especially in small children, after ingestion of raw or improperly cooked Rhodactis howesii (Tu, 1988).
    C) ANIMAL DATA
    1) In mice, the 2 hour LD50 of granulitoxin (isolated from the sea anemone Bunodosoma granulifera) was 400 +/- 83 micrograms/kilogram (Santana et al, 1998).

Maximum Tolerated Exposure

    A) SUMMARY
    1) The sting of even one anemone may produce significant symptoms.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) CONGESTIN
    B) EQUINATOXIN
    C) THALASSIN

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Stinging anemones like the Anemonia sulcata are a coelenterate which contain nematocysts or "stinging capsules" (Fisher, 1999). These capsules contain the toxic substance of the coelenterate. Upon contact with the spirally-coiled thread with barbed endings, the toxin is forcibly ejected into the skin. The amount of toxic substance introduced varies widely among species. Discharge by a nematocyst requires both mechanical (friction) and chemical (fresh water) stimulation.

Toxicologic Mechanism

    A) Sea anemone venom from the tentacles of Anemonia sulcata is thought to contain several different fractions (Beress et al, 1975; Cariello & D'Aniello, 1975).
    1) Early experiments showed that when dogs were given a sensitizing dose of under 0.15 mL/kg of actinotoxin (toxin from Anemonia sulcata), they became sick, then recovered (Halsead, 1978).
    a) If these dogs were given another dose of 0.08 to 0.25 mL of the toxin within the next two weeks, they began to vomit, had dyspnea, foaming at the mouth, bloody diarrhea, pruritus, and died within a few hours.
    2) THALASSIN - The first of these venom fractions was called thalassin (Richet, 1902; Richet, 1904b). When injected into dogs, it produced nervousness, redness, urticaria, genital excitement, vasodilatation, facial edema, urticaria, pruritus, rhinitis, conjunctivitis, coughing, cardiac arrest, and death.
    a) Thalassin is especially pruritogenic. It is found in many marine animals besides this anemone (Halstead, 1978).
    3) CONGESTIN - Another of these sea anemone tentacle venoms was identified by Richet (1903, 1904a) and called congestin. When intravenously given to dogs, it produced vomiting, bloody diarrhea, abdominal pain, intense splanchnic vasodilatation, respiratory paralysis, hypotension, and death.
    a) If re-injected into the dogs within a 2 to 3 month period, this fraction produced an anaphylactic reaction and death (Portier & Richet, 1902b; Richet, 1904a; Richet, 1905a). If a small dose of thalassin is given first, the dog is able to tolerate larger doses of congestin.
    4) HYPNOTOXIN - Is found in some jellyfish tentacles and is thought to be in anemone venom. It produces CNS depression affecting both motor and sensory areas.
    a) Symptoms include coma, muscular paralysis, inactivity, and cutaneous anesthesia. Death occurs from respiratory paralysis (Portier & Richet, 1902a; Portier & Richet, 1902b).
    5) Another toxin, of low molecular weight, was isolated from Anemonia sulcata. It was a protein that was destroyed after heating to 90 degrees Centigrade for 15 minutes (Novak et al, 1973).
    B) PAIN - May be due to 5-hydroxytryptamine, a substance that can produce pain and release histamine (Welsh, 1956; Payne JH, 1961). Thalassin will also release histamine (Jaques & Schachter, 1954).
    C) EQUINATOXIN - Derived from Actinia equina was tested on rats. In less than a minute after injection of equinatoxin, respiration stopped and bradycardia occurred showing increased vagal tone (Sket et al, 1974).
    1) A transient fall in arterial blood pressure was noted, then an elevation of arterial blood pressure occurred.
    2) Various conduction disturbances, ectopic foci, myocardial ischemia, and negative inotropic and chronotropic effects were noted on the in-situ exposed heart (Sket et al, 1974).
    D) ANTHOPLEURA ELEGANTISSIMA EXTRACT - has shown activity against two experimental mouse tumors. It also displayed a positive inotropic effect on isolated rat atria (Quinn et al, 1974).
    E) POTASSIUM CHANNEL BLOCKERS - have been identified in the venoms of various anemones. Bunodosoma granulifera and Stichodactyla helianthus are examples (Karlsson et al, 1991).
    F) SODIUM CHANNEL TOXINS - which prevent the closing of sodium channels and prolong action potential, have been identified since the 1970s (Karlsson et al, 1991; Freitas & Malpezzi, 1991a).
    G) CYTOLYSINS - have been identified from various anemones. Radianthus macrodactylus is an example, producing a highly potent protein cytolysin (Shnyrov et al, 1991).

References

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